Circuitry to Assist with Neural Sensing in an Implantable Stimulator Device

ABSTRACT

Passive tissue biasing circuitry in an Implantable Pulse Generator (IPG) is disclosed to facilitate the sensing of neural responses by holding the voltage of the tissue to a common mode voltage (Vcm). The IPG&#39;s conductive case electrode, or any other electrode, is passively biased to Vcm using a capacitor, as opposed to actively driving the (case) electrode to a prescribed voltage using a voltage source. Once Vcm is established, voltages accompanying the production of stimulation pulses will be referenced to Vcm, which eases neural response sensing. An amplifier can be used to set a virtual reference voltage and to limit the amount of current that flows to the case during the production of Vcm. In other examples, circuitry can be used to monitor the virtual reference voltage as useful to enabling the sensing the neural responses, and as useful to setting a compliance voltage for the current generation circuitry.

CROSS REFERENCE TO RELATED APPLICATIONS

This is a non-provisional application of U.S. Provisional PatentApplication Ser. No. 62/650,844, filed Mar. 30, 2018, to which priorityis claimed, and which is incorporated herein by reference in itsentirety.

FIELD OF THE INVENTION

This application relates to Implantable Medical Devices (IMDs), and morespecifically to circuitry to assist with sensing in an implantablestimulator device.

INTRODUCTION

Implantable neurostimulator devices are devices that generate anddeliver electrical stimuli to body nerves and tissues for the therapy ofvarious biological disorders, such as pacemakers to treat cardiacarrhythmia, defibrillators to treat cardiac fibrillation, cochlearstimulators to treat deafness, retinal stimulators to treat blindness,muscle stimulators to produce coordinated limb movement, spinal cordstimulators to treat chronic pain, cortical and deep brain stimulatorsto treat motor and psychological disorders, and other neural stimulatorsto treat urinary incontinence, sleep apnea, shoulder subluxation, etc.The description that follows will generally focus on the use of theinvention within a Spinal Cord Stimulation (SCS) system, such as thatdisclosed in U.S. Pat. No. 6,516,227. However, the present invention mayfind applicability with any implantable neurostimulator device system.

An SCS system typically includes an Implantable Pulse Generator (IPG) 10shown in FIG. 1. The IPG 10 includes a biocompatible device case 12 thatholds the circuitry and a battery 14 for providing power for the IPG tofunction. The IPG 10 is coupled to tissue-stimulating electrodes 16 viaone or more electrode leads that form an electrode array 17. Forexample, one or more percutaneous leads 15 can be used havingring-shaped or split-ring electrodes 16 carried on a flexible body 18.In another example, a paddle lead 19 provides electrodes 16 positionedon one of its generally flat surfaces. Lead wires 20 within the leadsare coupled to the electrodes 16 and to proximal contacts 21 insertableinto lead connectors 22 fixed in a header 23 on the IPG 10, which headercan comprise an epoxy for example. Once inserted, the proximal contacts21 connect to header contacts 24 within the lead connectors 22, whichare in turn coupled by feedthrough pins 25 through a case feedthrough 26to stimulation circuitry 28 within the case 12.

In the illustrated IPG 10, there are thirty-two electrodes (E1-E32),split between four percutaneous leads 15, or contained on a singlepaddle lead 19, and thus the header 23 may include a 2×2 array ofeight-electrode lead connectors 22. However, the type and number ofleads, and the number of electrodes, in an IPG is application specificand therefore can vary. The conductive case 12 can also comprise anelectrode (Ec). In a SCS application, the electrode lead(s) aretypically implanted in the spinal column proximate to the dura in apatient's spinal cord, preferably spanning left and right of thepatient's spinal column. The proximal contacts 21 are tunneled throughthe patient's tissue to a distant location such as the buttocks wherethe IPG case 12 is implanted, at which point they are coupled to thelead connectors 22. In other IPG examples designed for implantationdirectly at a site requiring stimulation, the IPG can be lead-less,having electrodes 16 instead appearing on the body of the IPG 10 forcontacting the patient's tissue. The IPG lead(s) can be integrated withand permanently connected to the IPG 10 in other solutions. The goal ofSCS therapy is to provide electrical stimulation from the electrodes 16to alleviate a patient's symptoms, such as chronic back pain.

IPG 10 can include an antenna 27 a allowing it to communicatebi-directionally with a number of external devices discussedsubsequently. Antenna 27 a as shown comprises a conductive coil withinthe case 12, although the coil antenna 27 a can also appear in theheader 23. When antenna 27 a is configured as a coil, communication withexternal devices preferably occurs using near-field magnetic induction.IPG 10 may also include a Radio-Frequency (RF) antenna 27 b. In FIG. 1,RF antenna 27 b is shown within the header 23, but it may also be withinthe case 12. RF antenna 27 b may comprise a patch, slot, or wire, andmay operate as a monopole or dipole. RF antenna 27 b preferablycommunicates using far-field electromagnetic waves, and may operate inaccordance with any number of known RF communication standards, such asBluetooth, Zigbee, WiFi, MICS, and the like.

Stimulation in IPG 10 is typically provided by pulses each of which mayinclude a number of phases such as 30 a and 30 b, as shown in theexample of FIG. 2A. Stimulation parameters typically include amplitude(current I, although a voltage amplitude V can also be used); frequency(F); pulse width (PW) of the pulses or of its individual phases such as30 a and 30 b; the electrodes 16 selected to provide the stimulation;and the polarity of such selected electrodes, i.e., whether they act asanodes that source current to the tissue or cathodes that sink currentfrom the tissue. These and possibly other stimulation parameters takentogether comprise a stimulation program that the stimulation circuitry28 in the IPG 10 can execute to provide therapeutic stimulation to apatient.

In the example of FIG. 2A, electrode E1 has been selected as an anode(during its first phase 30 a), and thus provides pulses which source apositive current of amplitude +I to the tissue. Electrode E2 has beenselected as a cathode (again during first phase 30 a), and thus providespulses which sink a corresponding negative current of amplitude −I fromthe tissue. This is an example of bipolar stimulation, in which only twolead-based electrodes are used to provide stimulation to the tissue (oneanode, one cathode). However, more than one electrode may be selected toact as an anode at a given time, and more than one electrode may beselected to act as a cathode at a given time.

IPG 10 as mentioned includes stimulation circuitry 28 to form prescribedstimulation at a patient's tissue. FIG. 3 shows an example ofstimulation circuitry 28, which includes one or more current sourcecircuits 40 _(i) and one or more current sink circuits 42 _(i). Thesources and sinks 40 _(i) and 42 _(i) can comprise Digital-to-Analogconverters (DACs), and may be referred to as PDACs 40 _(i) and NDACs 42_(i) in accordance with the Positive (sourced, anodic) and Negative(sunk, cathodic) currents they respectively issue. In the example shown,a NDAC/PDAC 40 _(i)/42 _(i) pair is dedicated (hardwired) to aparticular electrode node ei 39. Each electrode node ei 39 is connectedto an electrode Ei 16 via a DC-blocking capacitor Ci 38, for the reasonsexplained below. The stimulation circuitry 28 in this example alsosupports selection of the conductive case 12 as an electrode (Ec 12),which case electrode is typically selected for monopolar stimulation.PDACs 40 _(i) and NDACs 42 _(i) can also comprise voltage sources.

Proper control of the PDACs 40 _(i) and NDACs 42 _(i) allows any of theelectrodes 16 to act as anodes or cathodes to create a current through apatient's tissue, R, hopefully with good therapeutic effect. In theexample shown, electrode E1 has been selected as an anode electrode tosource current to the tissue R and E2 as a cathode electrode to sinkcurrent from the tissue R. Thus PDAC 40 ₁ and NDAC 42 ₂ are activatedand digitally programmed to produce the desired current, I, with thecorrect timing (e.g., in accordance with the prescribed frequency F andpulse widths PWa and PWb). Power for the stimulation circuitry 28 isprovided by a compliance voltage VH, as described in further detail inU.S. Patent Application Publication 2013/0289665. As shown thecompliance voltage may be coupled to the source circuitry (e.g., thePDAC(s)), while ground may be coupled to the sink circuitry (e.g., theNDAC(s)), such that the stimulation circuitry is coupled to and poweredbetween the compliance voltage and ground. More than one anode electrodeand more than one cathode electrode may be selected at one time, andthus current can flow through the tissue R between two or more of theelectrodes 16.

Other stimulation circuitries 28 can also be used in the IPG 10. In anexample not shown, a switching matrix can intervene between the one ormore PDACs 40 _(i) and the electrode nodes ei 39, and between the one ormore NDACs 42 _(i) and the electrode nodes. Switching matrices allowsone or more of the PDACs or one or more of the NDACs to be connected toone or more anode electrode nodes at a given time. Various examples ofstimulation circuitries can be found in U.S. Pat. Nos. 6,181,969,8,606,362, 8,620,436, U.S. Patent Application Publication 2018/0071520,and U.S. patent application Ser. No. 16/131,809, filed Sep. 14, 2018.

Much of the stimulation circuitry 28 of FIG. 3, including the PDACs 40_(i) and NDACs 42 _(i), the switch matrices (if present), and theelectrode nodes ei 39 can be integrated on one or more ApplicationSpecific Integrated Circuits (ASICs), as described in U.S. PatentApplication Publications 2012/0095529, 2012/0092031, and 2012/0095519.As explained in these references, ASIC(s) may also contain othercircuitry useful in the IPG 10, such as telemetry circuitry (forinterfacing off chip with telemetry antennas 27 a and/or 27 b),circuitry for generating the compliance voltage VH, various measurementcircuits, etc.

Also shown in FIG. 3 are DC-blocking capacitors Ci 38 placed in seriesin the electrode current paths between each of the electrode nodes ei 39and the electrodes Ei 16 (including the case electrode Ec 12). TheDC-blocking capacitors 38 act as a safety measure to prevent DC currentinjection into the patient, as could occur for example if there is acircuit fault in the stimulation circuitry 28, and also generallycomprise part of the IPG's charge balancing mechanism. The DC-blockingcapacitors 38 are typically provided off-chip (off of the ASIC(s)), andinstead may be provided in or on a circuit board in the IPG 10 used tointegrate its various components, as explained in U.S. PatentApplication Publication 2015/0157861.

Referring again to FIG. 2A, the stimulation pulses as shown arebiphasic, with each pulse comprising a first phase 30 a followedthereafter by a second phase 30 b of opposite polarity. Biphasic pulsesare useful to actively recover any charge that might be stored oncapacitive elements in the electrode current paths, such as on theDC-blocking capacitors 38. Charge recovery is shown with reference toboth FIGS. 2A and 2B. During the first pulse phase 30 a, charge will(primarily) build up across the DC-blockings capacitors C1 and C2associated with the electrodes E1 and E2 used to produce the current,giving rise to voltages Vc1 and Vc2 (I=C*dV/dt). During the second pulsephase 30 b, when the polarity of the current I is reversed at theselected electrodes E1 and E2, the stored charge on capacitors C1 and C2is recovered, and thus voltages Vc1 and Vc2 hopefully return to 0V atthe end the second pulse phase 30 b.

To recover all charge by the end of the second pulse phase 30 b of eachpulse (Vc1=Vc2=0V), the first and second phases 30 a and 30 b arecharged balanced at each electrode, with the phases comprising an equalamount of charge but of the opposite polarity. In the example shown,such charge balancing is achieved by using the same pulse width(PWa=PWb) and the same amplitude (|+I|=|−I|) for each of the pulsephases 30 a and 30 b. However, the pulse phases 30 a and 30 b may alsobe charged balance if the product of the amplitude and pulse widths ofthe two phases 30 a and 30 b are equal, as is known.

FIG. 4 shows various external devices that can wirelessly communicatedata with the IPG 10, including a patient, hand-held external controller60, and a clinician programmer 70. Both of devices 60 and 70 can be usedto wirelessly transmit a stimulation program to the IPG 10—that is, toprogram its stimulation circuitry 28 to produce stimulation with desiredamplitudes and timings as described earlier. Both devices 60 and 70 mayalso be used to adjust one or more stimulation parameters of astimulation program that the IPG 10 is currently executing. Devices 60and 70 may also wirelessly receive information from the IPG 10, such asvarious status information, etc. Devices 60 and 70 may additionallycommunicate with an External Trial Stimulator (ETS) which is used tomimic operation of the IPG 10 during a trial period and prior to theIPG's implantation, as explained in U.S. Pat. Nos. 9,724,508 and9,259,574.

External controller 60 can be as described in U.S. Patent ApplicationPublication 2015/0080982 for example, and may comprise a controllerdedicated to work with the IPG 10. External controller 60 may alsocomprise a general purpose mobile electronics device such as a mobilephone which has been programmed with a Medical Device Application (MDA)allowing it to work as a wireless controller for the IPG 10, asdescribed in U.S. Patent Application Publication 2015/0231402. Externalcontroller 60 includes a user interface, preferably including means forentering commands (e.g., buttons or selectable graphical icons) and adisplay 62. The external controller 60's user interface enables apatient to adjust stimulation parameters, although it may have limitedfunctionality when compared to the more-powerful clinician programmer70, described shortly.

The external controller 60 can have one or more antennas capable ofcommunicating with the IPG 10. For example, the external controller 60can have a near-field magnetic-induction coil antenna 64 a capable ofwirelessly communicating with the coil antenna 27 a in the IPG 10. Theexternal controller 60 can also have a far-field RF antenna 64 b capableof wirelessly communicating with the RF antenna 27 b in the IPG 10.

Clinician programmer 70 is described further in U.S. Patent ApplicationPublication 2015/0360038, and can comprise a computing device 72, suchas a desktop, laptop, or notebook computer, a tablet, a mobile smartphone, a Personal Data Assistant (PDA)-type mobile computing device,etc. In FIG. 4, computing device 72 is shown as a laptop computer thatincludes typical computer user interface means such as a screen 74, amouse, a keyboard, speakers, a stylus, a printer, etc., not all of whichare shown for convenience. Also shown in FIG. 4 are accessory devicesfor the clinician programmer 70 that are usually specific to itsoperation as a stimulation controller, such as a communication “wand” 76coupleable to suitable ports on the computing device 72, such as USBports 79 for example.

The antenna used in the clinician programmer 70 to communicate with theIPG 10 can depend on the type of antennas included in the IPG 10. If thepatient's IPG 10 includes a coil antenna 27 a, wand 76 can likewiseinclude a coil antenna 80 a to establish near-filed magnetic-inductioncommunications at small distances. In this instance, the wand 76 may beaffixed in close proximity to the patient, such as by placing the wand76 in a belt or holster wearable by the patient and proximate to thepatient's IPG 10. If the IPG 10 includes an RF antenna 27 b, the wand76, the computing device 72, or both, can likewise include an RF antenna80 b to establish communication with the IPG 10 at larger distances. Theclinician programmer 70 can also communicate with other devices andnetworks, such as the Internet, either wirelessly or via a wired linkprovided at an Ethernet or network port.

To program stimulation programs or parameters for the IPG 10, theclinician interfaces with a clinician programmer graphical userinterface (GUI) 82 provided on the display 74 of the computing device72. As one skilled in the art understands, the GUI 82 can be rendered byexecution of clinician programmer software 84 stored in the computingdevice 72, which software may be stored in the device's non-volatilememory 86. Execution of the clinician programmer software 84 in thecomputing device 72 can be facilitated by control circuitry 88 such asone or more microprocessors, microcomputers, FPGAs, DSPs, other digitallogic structures, etc., which are capable of executing programs in acomputing device, and which may comprise their own memories. Suchcontrol circuitry 88, in addition to executing the clinician programmersoftware 84 and rendering the GUI 82, can also enable communications viaantennas 80 a or 80 b to communicate stimulation parameters chosenthrough the GUI 82 to the patient's IPG 10.

The user interface of the external controller 60 may provide similarfunctionality because the external controller 60 can include similarhardware and software programming as the clinician programmer. Forexample, the external controller 60 includes control circuitry 66similar to the control circuitry 88 in the clinician programmer 70, andmay similarly be programmed with external controller software stored indevice memory.

SUMMARY

An implantable stimulator device is disclosed, which may comprise: aplurality of electrode nodes, each electrode node configured to becoupled to one of a plurality of electrodes configured to contact apatient's tissue; a case configured for implantation in the patient'stissue, where the case contains stimulation circuitry configured toprovide pulses at at least two of the electrode nodes to create astimulation current through the patient's tissue; and a capacitanceconfigured to be coupled between at least one of the plurality ofelectrodes and a first reference voltage produced inside the case whenthe stimulation circuitry is providing the pulses to the at least twoelectrode nodes, where the capacitance is configured to provide a commonmode voltage to the tissue at the at least one electrode.

The case may be conductive, and the conductive case may comprise one ofthe plurality of electrodes. The conductive case may comprise the atleast one electrode.

The at least one electrode may be configured to be selectable from theplurality of electrodes.

The implantable stimulator device may further comprise a resistor inparallel with the capacitance.

The capacitance may comprise one or more capacitors.

Each electrode node may be coupled to an electrode through a DC-blockingcapacitor.

The stimulation circuitry may be further configured to provide pulses tothe at least one electrode, where the capacitance is configured to beuncoupled between the at least one electrode and the first referencevoltage when the stimulation circuitry is providing the pulses to the atleast one electrode.

The implantable stimulator device may further comprise at least oneimplantable lead, where the electrodes are located on the lead. Theimplantable stimulator device may also further comprise a switchconfigured to couple the capacitance to the first reference voltage. Theimplantable stimulator device may also further comprise a voltage sourceconfigured to produce the first reference voltage.

The stimulation circuitry may be configured to be powered by acompliance voltage. The stimulation may comprise source circuitryconfigured to source a current to at least one of the two electrodes,and sink circuitry configured to sink a current from a different atleast one of the two electrodes. The compliance voltage may be coupledto the source circuitry, and a ground may be coupled to the current sinkcircuitry. The first reference voltage may be between the compliancevoltage and a ground, or may be configured to scale with the compliancevoltage.

The implantable stimulator device may further comprise an amplifierconfigured to produce the first reference voltage. The amplifier maycomprise an operational transconductance amplifier. The amplifier maycomprise a first input and a second input, and may be configured as afollower in which the first reference voltage is provided to the firstinput, and where a second reference voltage is provided to the secondinput. The implantable stimulator device may further comprise a voltagesource configured to produce the second reference voltage. Thestimulation circuitry may be configured to be powered by a compliancevoltage. The second reference voltage may be between the compliancevoltage and a ground, or may be configured to scale with the compliancevoltage. The amplifier may be configured to maintain the first referencevoltage equal to the second reference voltage if a current through thecapacitance is between a minimum and maximum output current of theamplifier.

The implantable stimulator device may further comprise logic circuitryconfigured to determine whether the first reference voltage exceeds afirst threshold or falls below a second threshold. The implantablestimulator device may further comprise control circuitry configured toreceive at least one indication that the first reference voltage hasexceeded the first threshold or has fallen below the second threshold.The control circuitry may be configured in response to the at least oneindication to issue an enable signal indicating when a neural responsein the tissue in response to the stimulation current can be sensed at atleast one of the plurality of electrode nodes. The stimulation circuitrymay be powered by a compliance voltage, where the control circuitry isconfigured in response to the at least one indication to issue an enablesignal indicating when the compliance voltage should be increased.

The implantable stimulator device may further comprise at least onesense amplifier configured to sense a neural response in the tissue inresponse to the stimulation current when the capacitance is configuredto provide the common mode voltage to the tissue at the at least oneelectrode. The at least one sense amplifier may comprise a first inputand a second input, where the at least one sense amplifier is configuredto receive one of the electrode nodes at its first input. The oneelectrode node received at the first input may not comprise one of theat least two of the electrode nodes. The at least one sense amplifiermay be configured to receive the common mode voltage at its secondinput. The at least one sense amplifier may also be configured toreceive another one of the electrode nodes at its second input todifferentially sense the neural response between the one electrode nodeand the another electrode node. The implantable stimulator device mayfurther comprise control circuitry configured to receive an output ofthe at least one sense amplifier and to assess at least one parameter ofthe sensed neural response.

BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1 shows an Implantable Pulse Generator (IPG), in accordance withthe prior art.

FIGS. 2A and 2B show an example of stimulation pulses producible by theIPG, in accordance with the prior art.

FIG. 3 shows stimulation circuitry useable in the IPG, in accordancewith the prior art.

FIG. 4 shows various external devices capable of communicating with andprogramming stimulation in an IPG, in accordance with the prior art.

FIG. 5 shows an improved IPG having neural response sensing, and theability to adjust stimulation dependent on such sensing.

FIG. 6 shows stimulation producing a neural response, and the sensing ofthat neural response at at least one electrode of the IPG.

FIGS. 7A and 7B show the production of biphasic pulses at selected IPGelectrodes, and shows the voltages formed at the selected electrodenodes.

FIGS. 8A and 8B show the problem of insufficient compliance voltageproducing stimulation pulses that are loaded, and show circuitry foradjusting the compliance voltage to prevent loading in a closed loopfashion.

FIGS. 9A and 9B show first examples of passive tissue biasing circuitryconfigured to establish a common mode voltage in the tissue at the caseelectrode using a capacitor, as useful for example in the sensing ofneural responses.

FIGS. 10A and 10B explain operation of the passive tissue biasingcircuitry in establishing the common mode voltage in the tissue.

FIGS. 11A-11C explain operation of the passive tissue biasing circuitrygiven potential mismatches in electrode-to-case resistance andmismatches between the source and sunk current in the tissue.

FIGS. 12A and 12B show a second example of passive tissue biasingcircuitry including an amplifier for producing a virtual referencevoltage for the capacitor and for limiting the current through thetissue to the case.

FIGS. 13A and 13B show a third example of passive tissue biasingcircuitry including circuitry to sense the virtual reference voltage ashelpful to enabling sensing of neural responses, and as helpful toadjusting the compliance voltage for the current generation circuitry.

FIGS. 14A and 14B show sensing of a neural response at both a singleelectrode and differentially at two electrodes once the common modevoltage is established.

FIG. 15 shows an alternative in which the passive tissue biasingcircuitry can allow any electrode (beyond the case electrode) tocomprise the electrode used to set the common mode voltage in thetissue.

DETAILED DESCRIPTION

An increasingly interesting development in pulse generator systems, andin Spinal Cord Stimulator (SCS) pulse generator systems specifically, isthe addition of sensing capability to complement the stimulation thatsuch systems provide. For example, and as explained in U.S. PatentApplication Publication 2017/0296823, it can be beneficial to sense aneural response in neural tissue that has received stimulation from anSCS pulse generator.

FIG. 5 shows circuitry for an SCS IPG 100 having neural response sensingcapability. The IPG 100 includes control circuitry 102, which maycomprise a microcontroller for example, such as Part Number MSP430,manufactured by Texas Instruments, which is described in data sheets athttp://www.ti.com/lsds/ti/microcontroller/16-bit_msp430/overview.page?DCMP=MCU_other&HQS=msp430. Other types of control circuitry may be used in lieu of amicrocontroller as well, such as microprocessors, FPGAs, DSPs, orcombinations of these, etc. Control circuitry 102 may also be formed inwhole or in part in one or more Application Specific Integrated Circuits(ASICs) in the IPG 100 as described earlier, which ASIC(s) mayadditionally include the other circuitry shown in FIG. 5.

FIG. 5 includes the stimulation circuitry 28 described earlier (FIG. 3),including one or more DACs (PDACs 40 _(i) and NDACs 42 _(i)). A bus 118provides digital control signals to the DACs to produce currents orvoltages of prescribed amplitudes and with the correct timing at theelectrodes selected for stimulation. The electrode current paths to theelectrodes 16 include the DC-blocking capacitors 38 described earlier.

The control circuitry 102 is programmed with a neural response algorithm124 to evaluate a neural response of neurons that fire (are recruited)by the stimulation that the IPG 100 provides. One such neural responsedepicted in FIGS. 5 and 6 is an Evoked Compound Action Potential, or“ECAP,” although other types of neural responses also exist and can besensed by the IPG 100. As its name implies, an ECAP comprises a compound(summation) of various action potentials issued from a plurality ofrecruited neurons, and its amplitude and shape varies depending on thenumber and type of neural fibers that are firing. Generally speaking, anECAP can vary between tens of microVolts to tens of milliVolts. Theneural response algorithm 124 assesses the ECAP and can, for example,adjust the stimulation program in a closed loop fashion to try andadjust the amplitude or shape of the resulting ECAP.

The control circuitry 102 and/or the neural response algorithm 124 canalso enable one or more sense electrodes (S) to sense the ECAP, eitherautomatically or based on a user selection of the sense electrode(s) asentered into an external device (see FIG. 4). As shown in FIG. 6, theECAP will be initiated upon stimulation of neural fibers in a recruitedneural population 95 proximate to the electrodes chosen for stimulation(e.g., E1 and E2), and will move through the patient's tissue via neuralconduction. In the simple example of FIG. 6, electrode E6 is chosen as asense electrode S, and thus this electrode will detect the ECAP as itmoves past. The speed at which the ECAP moves depends on the severalfactors, and is variable.

To assist with selection of the sensing electrode(s), and referringagain to FIG. 5, each electrode node ei 39 is made coupleable to atleast one sense amp 110. In this example, for simplicity, all of theelectrode nodes are shown as sharing a single sense amp 110. Thus, anyone sensing electrode (e.g., electrode node e6) can be coupled to thesense amp 110 (e.g., Ve6) at a given time per multiplexer 108, ascontrolled by bus 114. However, although not shown, each electrode nodecan also be coupleable to its own dedicated sense amp 110. ECAP sensingcan also involve differential sensing of the ECAP at more than oneelectrode (e.g., at electrodes E5 and E6), and thus two electrode nodes(e.g., Ve5 and Ve6) can be input to a differential sense amp 110; thisis explained later with reference to FIG. 14B, but isn't shown in FIGS.5 and 6 for simplicity. After the ECAP is sensed, the analog waveformcomprising the ECAP is preferably converted to digital signals by anAnalog-to-Digital converter 112, which may also reside within thecontrol circuitry 102. The neural response algorithm 124 can then assessthe amplitude and shape of the ECAP, and if necessary make adjustmentsto stimulation via bus 118 to try and adjust resulting future ECAPs sothat they have desired amplitudes or shapes.

The sensing electrode(s) S may be distant from the active electrodeschosen to provide stimulation so that voltages created in the tissueduring stimulation (stimulation artifacts) will less affect sensing atthe sensing electrode. Nonetheless, because the duration (e.g., PWa andPWb) and frequency (F) of the stimulation pulses and the conductionspeed of neural responses are variable, it may be inevitable thatstimulation-related voltages are present at the sensing electrode(s)chosen. This can make sensing neural responses challenging. As noted, anECAP can be as small as tens of microVolts. However, as explainedfurther below, operation of the IPG can cause the voltage in the tissueto vary on the order of Volts. Sensing thus involves resolving a smallsignal neural response in the tissue that may be many orders ofmagnitudes smaller than the varying background voltage of the tissue. Itis difficult to design an amplifier such as sense amp(s) 110 to reliablyperform the task of accurately sensing such a small signal whilerejecting the background tissue voltage.

Voltage variation in the tissue due to stimulation is first explainedwith reference to FIGS. 7A and 7B, which show stimulation occurringusing biphasic pulses between electrodes E1 and E2 as described earlier.FIG. 7A shows how the stimulation circuitry 28 is biased when producinga current I through the tissue during the first phase 30 a when currentI travels from anode electrode E1 to cathode electrode E2, and duringthe second phase 30 b when current I travels in the opposite directionfrom anode electrode E2 to cathode electrode E1. Note during the firstphase 30 a that a selected PDAC (e.g., PDAC 40 ₁) sources current Ip toelectrode node e1 while a selected NDAC (e.g., NDAC 42 ₂) sinks currentIn from electrode node e2. During the second phase 30 b, a selected PDAC(e.g., PDAC 40 ₂) sources current Ip to electrode node e2 and a selectedNDAC (e.g., NDAC 42 ₁) sinks current In from electrode node e1. Ideally,Ip issued from the PDACs equals issued by the NDACs, with both equalingthe desired current I, although non-idealities may cause them to vary asdiscussed further below. The same PDAC and NDAC could also be usedduring the two phases 30 a and 30 b if switch matrices are used as partof the design of stimulation circuitry 28.

FIG. 7B shows various waveforms that are produced when biphasic currentpulses are produced at electrodes E1 and E2. Providing a constantcurrent I between the electrodes causes the DC-blocking capacitors 38 C1and C2 to charge during the first pulse phases 30 a, which causes thevoltages across them Vc1 and Vc2 to increase (I=C*dV/dt). Because thesecond pulse phase 30 b of opposite polarity is charge balanced with thefirst pulse phase 30 a, Vc1 and Vc2 will decrease during the secondpulse phases 30 b and return (ideally) to zero at the end of the secondpulse phase 30 b, as explained earlier with reference to FIGS. 2A and2B.

The bottom of FIG. 7B shows the voltages that are formed at theelectrode nodes 39 e1 and e2 (Ve1 and Ve2) when producing the foregoingpulses. It is useful to review the voltages at the electrode nodes 39 eirather than at the electrodes Ei 16 themselves because it is thevoltages at the electrode nodes that are presented to the sense amp(s)110 (FIG. 5) and hence used for neural response sensing. Even though Ve1and Ve2 are formed at the same time, they are initially shown separatelyin FIG. 7B for simplicity, with the first waveform showing just Ve1during a first pulse, and the second waveform showing just Ve2 during asecond pulse. The third waveform shows Ve1 and Ve2 together during athird pulse.

The electrode node voltages Ve1 and Ve2 in FIG. 7B are shown withreference to the compliance voltage VH that as mentioned earlier (FIG.3) is used to provide power to the DAC circuitry. All relevant voltagedrops are shown, including the voltage drops across the tissue (Vr), theDC-blocking capacitors 39 (Vc1 and Vc2), and the selected PDACs andNDACs (Vp and Vn). As shown, Ve1 is initially higher than Ve2 because ofthe direction that the current is flowing during the first pulse phase30 a. Ve1 will increase and Ve2 will decrease during the first pulsephase 30 a as the DC-blocking capacitors 38 charge (Vc1, Vc2). This alsocauses the voltage drops across the active PDAC (Vp) and NDAC (Vn) todecrease. During the second pulse phase 30 b, the polarity of thecurrent is reversed, and so Ve2 is now higher than Ve1. The voltages Vc2and Vc2 decrease during the second pulse phase 30 b as their storedcharge is recovered, which causes Ve1 to decrease and Ve2 to increase,while Vp and Vn decrease.

Voltages Ve1 and Ve2 thus vary significantly during the issuance of thebiphasic pulses, both because of the change in polarity of the current,and the charging and discharging of the DC-blocking capacitors 38. Suchvariation is indicative of variation of voltage in the tissue, whichvoltage will couple to at least some degree through the tissue to theelectrodes that are used for sensing. Assume again that sensing is tooccur at electrode E6—i.e., that sensed voltage Ve6 is presented to thesense amp(s) 110. Although it is complicated to calculate or graph giventhe complicated electrical environment of the tissue, voltages presentat electrodes E1 and E2 will couple to electrode E6, and thus Ve6 willgenerally track Ve1 and/or Ve2 to some degree. (In this example, Ve6would likely primarily track Ve2 because electrode E6 is closer to E2than E1). In other words, any small signal neural response sensed at Ve6will be riding on a large and varying background voltage, which as notedearlier makes sensing of the neural response difficult. As will bedescribed further below, the addition of passive tissue biasingcircuitry to the IPG 100 will provide a common mode voltage to thetissue which eases the sensing of small signal neural responses.

Before discussing such passive tissue biasing circuitry, it is useful todiscuss how the compliance voltage VH can be adjusted in the IPG 100,because such adjustment can be implicated by the operation of thepassive tissue biasing circuitry. Compliance voltage adjustment, andcircumstances in which such adjustment is warranted, are shown in FIGS.8A and 8B. When providing stimulation, the voltage drops Vp and Vnacross the PDACs and NDACs are preferably held above minimum valuesVp(min) and Vn(min), as explained in U.S. Pat. Nos. 7,444,181, 9,174,051and 9,314,632. If Vp or Vn drop below these minimum values, the affectedDAC, either the PDAC or NDAC, will become loaded and thus will be unableto produce its prescribed current Ip or In. This means that Ve1 and Ve2preferably stay bounded within a region 111 between VH-Vp(min) andVn(min). In the example of FIG. 8A, such bounding does not occur,because Ve2<Vn(min) and Ve1>VH-Vp(min) during part (98) of the firstpulse phase 30 a. This leads to loading (99) of the pulses because thePDAC(s) and NDAC(s) are unable to produce the prescribed currents of Ipand In.

While the compliance voltage may be constant, it is also preferablyadjustable to address pulse loading, and FIG. 8B shows an example ofcompliance voltage measurement and generation circuitry 51 that can beused for this purpose. Generally speaking, compliance voltagemeasurement and generation circuitry 51 measures Vp and Vn across theactive PDACs and NDACs, and adjusts the compliance voltage VH in aclosed loop fashion to ensure that Vp does not fall below Vp(min) andthat Vn does not fall below Vn(min), thus ensuring that the electrodenode voltages Ve1 and Ve2 are bounded by region 111.

As shown, differential amplifiers 43 p and 43 n measure Vp and Vn acrossthe active PDAC 40 ₁ and NDAC 42 _(j) during provision of the pulse (I).Note that FIG. 8B only shows measuring Vp and Vn across PDAC 40 ₁ andNDAC42 ₂ during the first pulse phase 30 a. Vp and Vn can also bemeasured across PDAC 40 ₂ and NDAC 42 ₁ during the second pulse phase 30b, although this is not shown.

The Vp and Vn measurements are provided to negative inputs ofcomparators 45 p and 45 n. The comparators' positive inputs are providedwith the minimum values of Vp and Vn (Vp(min) and Vn(min)) needed acrossthe PDAC and NDAC to prevent loading. Vp(min) and Vn(min) can bedifferent owing to differences in the construction of the PDACs andNDACs, and may for example be 1.5 V and 1.2V respectively. Vp(min) andVn(min) can be provided by voltage generators such as bandgap voltagereference generators, although this detail isn't shown. Comparator 45 pis enabled by signal p(en) to compare Vp and Vp(min) at a prescribedtime, such as at the end of the first pulse phase 30 a when Vc1 and Vc2may be highest, and thus when Vp may be lowest. Comparator 45 n issimilarly enabled by signal n(en) to compare Vn and Vn(min) at theprescribed time when Vn may also be lowest. Comparators 45 p and 45 nwill output a ‘1’ if Vp is lower than Vp(min) or if Vn is lower thanVn(min). An OR gate 47 outputs a ‘1’ if either Vp or Vn is low, whichoutput signal comprises an enable signal VH(en1) to operate a compliancevoltage regulator 49.

The compliance voltage (VH) regulator 49 is shown in this example as aninductor-based boost converter, but could also be implemented as acapacitor-based charge pump or other voltage-boosting circuitry. VHregulator 49 produces the compliance voltage VH from anothertypically-lower-voltage DC source in the IPG 100 such as the voltage ofits battery 14 (FIG. 1), Vbat. When enabled by VH(en1) at input VH(en),a pulse width modulator 53 produces a square wave to a gating transistor57, which periodically turns on the transistor 57 and causes current toflow from Vbat through an inductor 55. During off periods of thetransistor 57, stored current in the inductor 55 is forced through adiode 59, and is stored on a storage capacitor 61 that holds the valueof the compliance voltage VH. The diode 59 prevents the backflow of thiscurrent, and so over time, the voltage across the storage capacitor 61increases, i.e., the compliance voltage VH, starts to build so long asVH(en1) continues to be asserted. Eventually, VH will increase to apoint that Vp and Vn are brought above Vp(min) and Vn(min), which willcause VH(en1) to deassert, which turns off the VH regulator 49 andallows VH to fall. As such, VH is controlled to an optimal level in aclosed loop fashion by compliance voltage measurement and generationcircuitry 51.

Operation of the compliance voltage measurement and generation circuitry51 of FIG. 8B can thus prevent loading 99 of the pulses by increasingthe compliance voltage VH, as illustrated in FIG. 8A. Note that after VHhas been raised, Ve1 nor Ve2 stay bounded within region 111, which keepsthe pulses from loading (99).

Various examples of the invention disclose passive tissue biasingcircuitry which can mitigate the effect of voltage variation in thetissue, and therefore facilitate the sensing of neural responses, bypassively holding the voltage of the tissue to a common mode voltage(Vcm). In examples of the invention, the IPG 100's conductive caseelectrode 12 is passively biased to Vcm using a capacitor, as opposed toactively driving the case electrode 12 to a prescribed voltage using avoltage source. Using the case electrode 12 to provide Vcm, while notstrictly necessary, is sensible: a patient's tissue is of relatively lowresistance, and the IPG's case electrode 12 is relatively large in area.Therefore, even if the case electrode 12 is implanted at a distance fromthe electrodes 16, the case electrode 12 still comprises a suitablemeans for establishing Vcm for the whole of the tissue. The passivetissue biasing circuitry however can also cause any electrode of the IPG100, including the lead based electrodes 16, to set the common modevoltage of the tissue. Nonetheless, the bulk of this disclosure assumesuse of the case electrode to set Vcm as a primary example.

As explained below, once Vcm is established at the case electrode 12 andhence in the tissue, voltages otherwise formed in the tissue, such asthose accompanying the production of stimulation pulses, will beestablished relative to Vcm. This can ease sensing of small signals inthe tissue, such as the sensing of neural responses (e.g., ECAPs). Asexplained below, Vcm may not be perfectly constant (i.e., it may bepseudo-constant), but nonetheless may be made to vary to a small enoughdegree to ease sensing.

The case 12 that houses the stimulation circuitry and other componentsis preferably entirely conductive, but, although not shown, may only beconductive at a portion. For example, the conductive case 12 may beinsulative in parts, but conductive at a portion and able at suchportion to produce the common mode voltage Vcm. In other words, thedisclosed technique is effective even if the conductive case isn'tentirely conductive but conductive only in part.

A first example of passive tissue biasing circuitry 150 configured toestablish a common mode voltage Vcm in the tissue is shown in FIG. 9A.In this example, a capacitor Ccm 152 is provided between the caseelectrode Ec 12 at the capacitor's top plate and a reference voltageVref at the capacitor's bottom plate, the magnitude of which isdiscussed below. A current Icm may flow through capacitor Ccm to assistin passively setting Vcm, as described further below. Ccm may also moregenerally comprise a capacitance, which may be comprised of a singlecapacitor or one or more capacitors or capacitances. A reasonable valuefor Ccm can depend on many factors, such as the maximum allowed ripplefor Vcm, the degree of potential imbalance in the stimulation circuitry,and a maximum output current of an amplifier useable in the passivetissue biasing circuitry, all of which are discussed below. In anyevent, Ccm would typically range between 1 and 10 microFarads, and maycomprise 4.7 microFarads in one example.

The reference voltage Vref may comprise a constant voltage provided by avoltage source 153 inside the conductive case Ec 12. Vref may beadjustable, and preferably has a value between or equal to ground (0V)and the compliance voltage (VH). Vref may also have a value that variesas a function of the compliance voltage VH, which as noted earlier mayvary by operation of compliance voltage measurement and generationcircuitry 51 (FIG. 8B). For example, Vref may be set to VH/2. In justone example, a voltage source 153 producing VH/2 may be formed as avoltage divider comprising a resistor ladder with serially-connectedhigh resistances Ra, as shown to the right in FIG. 9A. The common modevoltage Vcm established in the tissue comprises the sum of any voltageacross capacitor Ccm 152 and Vref. Note that voltage source 153 is notstrictly necessary, particular if Vref equals zero, in which case theend of switch 154 (explained below) may simply be connected to ground.

Note that the tissue R between the case electrode Ec 12 and theelectrodes selected for stimulation (E1 and E2) has been represented asa resistor network comprising resistances Rc, R1, and R2 coupled toelectrodes Ec, E1, and E2. The relevance of this resistor network isdescribed further below with reference to FIGS. 11A-11C.

Also shown in FIG. 9A are aspects of the stimulation circuitry 28including the PDAC(s) 40 _(i) and NDAC(s) 42 _(i) connected to thevarious electrode nodes 39 ei. Such aspects of stimulation circuitry 28are useful to show, particularly as concerns the case electrode, becauseas mentioned above the case electrode node ec/case electrode Ec 12 canbe actively driven similarly to any other electrode 16 (e.g., duringmonopolar stimulation). However, such operation of the stimulationcircuitry 28 to actively drive the case electrode is inconsistent withoperation of passive tissue biasing circuitry 150, and so switches 156and 154 are provided to isolate the two circuits 28 and 150.

When it is desired to actively drive the case electrode Ec 12 usingstimulation circuitry 28 (e.g., PDAC40 _(C) or NDAC 42 _(C)), controlsignal A is asserted to close switch 156 to connect the stimulationcircuitry 28 to the case electrode Ec 12, and control signal B isdeasserted to open switch 154 to isolate capacitor Ccm 152 within thepassive tissue biasing circuitry 150 from the case electrode 12.Alternatively, when using the passive tissue biasing circuitry 150 topassively set the common mode voltage Vcm in the tissue, control signalB is asserted to close switch 154 to connect capacitor Ccm 152 withinthe passive tissue biasing circuitry 150 to the case electrode 12, andcontrol signal A is deasserted to open switch 156 to isolate thestimulation circuitry 28 from the case electrode 12. If the passivetissue biasing circuitry 150 need not operate, and if the case electrodeis not being driven by stimulation circuitry 28, both of switches 154and 156 can be open. Control signals A and B may be issued by thecontrol circuitry 102 (FIG. 5) in the IPG 100, and switches 154 and 156may also appear on the other side of their respective capacitors Ccm andCc, or on the other side of voltage source 153. In FIG. 9A andsubsequent figures, switch 154 is closed and switch 156 opened to focusdiscussion on operation of the passive tissue biasing circuitry 150.

Although not shown, activation of the passive tissue biasing circuitry150 (and disconnection of the stimulation circuitry 28 from the caseelectrode Ec), can be affected by programming the IPG 100. For example,during periods when the IPG 100 is to sense neural responses and whenneural response algorithm 124 (FIG. 5) is active, the control circuitry102 can automatically close switch 154 and open switch 156. Such sensingneed not always occur during operation of the IPG 100, and so thecontrol circuitry 102 can open switch 154 at other times, thus allowingthe case electrode Ec to be actively driven by the stimulation circuitry28 if desired. External devices in communication with the IPG 100, suchas the clinician programmer 70 or external controller 60 (FIG. 4), canalso be used to place the IPG 100 in a neural sensing mode which willclose switch 154 to allow the passive tissue biasing circuitry 150 tofunction to passively set a common mode voltage Vcm in the tissue. Userinterfaces of those devices 60 and 70 can have selectable options toaffect this.

FIG. 9B shows a variation to the passive tissue biasing circuitry 150′in which the DC-blocking capacitor Cc 38 between electrode node ec andelectrode Ec is also used as the capacitor Ccm 152 within the passivetissue biasing circuitry. Again, switches 154 and 156 and theirrespective control signals A and B allow either the passive tissuebiasing circuitry 150′ or the stimulation circuitry 28 to be connectedto the case electrode Ec 12.

FIGS. 10A and 10B explain operation of the passive tissue biasingcircuitry 150 or 150′ (both simply referred to subsequently as 150), andshow particularly how the circuitry operates if the PDAC(s) and NDAC(s)used to provide current pulses at the selected electrodes (again, E1 andE2 for illustration, but other electrodes can be chosen) have variationin the magnitudes of the currents Ip and In they provide (see FIG. 7A).As noted earlier, Ip and are ideally equal in magnitude at any giventime. But non-idealities may cause the amplitude of Ip and to differslightly, perhaps because of differences in PDAC and NDAC construction.Ip and may also simply turn on and off at slightly different times ifthere is variation in the timing of the control of the PDACs and NDACs.Finally, Ip may not equal if either of the PDACs or NDACs is notsufficiently powered, i.e., if the voltage drops Vp or Vn across themare not greater than or equal to Vp(min) or Vn(min) respectively. Asexplained earlier, Vp or Vn being too low can cause loading of thepulses (99, FIG. 8A), which may require enabling of the compliancevoltage measurement and generation circuitry 51 to raise the compliancevoltage (FIG. 8B).

The passive tissue biasing circuitry 150 is beneficial in its ability tohandle such non-idealities and to set common mode voltage Vcmaccordingly. In example 158 of FIG. 10A, it is assumed that Vref is setto zero Volts (e.g., voltage source 153 is not present). It is furtherassumed that Ip provided by the PDAC(s) is initially greater than thecurrent provided by the NDAC(s) (i.e., Ip>|In|). In this case, thedifference in these currents (Ip−|In|) comprises a positive current Icmthat will initially flow through the capacitor Ccm 152 from the caseelectrode Ec 12 to ground during each pulse phase 30 a and 30 b. Anycurrent Icm charges the capacitor Ccm 152, in this case with a positivevoltage, which initially increases Vcm during each pulse phase 30 a or30 b, as shown in FIG. 10A. (Vcm may decay slightly during quiet periods30 c between the pulses).

Establishing Vcm at the case electrode Ec, and hence in the tissue,causes electrode node voltages Ve1 and Ve2 to become referenced to thisvoltage. Thus, as Vcm rises, so too will Ve1 and Ve2 start to rise. Ve1and Ve2 will eventually increase to a point at which Ve1 will justbarely start in part 98 to exceed VH-Vp(min), as shown in waveform 160of FIG. 10A. At this point, and as discussed earlier (FIG. 8A), thevoltage drop Vp across the PDACs 40 ₁ and 40 ₂ becomes too small tosupport production of the slightly larger current Ip, causing minimalloading 99 of the first phase pulses 30 a for electrode E1. (Suchminimal loading 99 of the pulses would not significantly alter thestimulation therapy the pulses provide). Ip will thus eventually dropslightly to match the value of (at least from a time-averaged or totalcharge standpoint), at which time Icm will equal 0. (Notice that Ipbeing loaded 99 also causes In to become loaded, since they are equal atthis point). Icm=0 prevents capacitor Ccm from charging further, andthus Vcm is eventually established at a pseudo-constant level higherthan Vref (ground), as shown in FIG. 10A.

If the NDAC(s) current In is higher than the PDAC(s)'s current Ip (i.e.,|In|>Ip), Icm would flow as a negative current from ground to the caseelectrode Ec 12. This would establish Vcm as a negative voltage inexample 158 (Vcm<Vref=0), which may be undesirable from a circuitrystandpoint. To accommodate this possibility, in examples 162 a and 162 bof FIG. 10B, Vref is set by voltage source 153 to a value higher thanzero but less than the compliance voltage VH (i.e., 0<Vref<VH). Forexample, Vref may be set to VH/2.

With Vref so set, Vcm will initially be set to Vref. Electrode nodevoltages Ve1 and Ve2 are thus initially referenced to Vcm=Vref, as shownin the waveform 164 of FIG. 10B.

If Ip>|In| as in example 162 a, Icm will initially be positive causing apositive voltage to form across capacitor Ccm 152. The effect of passivetissue biasing circuitry 150 is then similar to what occurred in example158 of FIG. 10A: Vcm will rise from Vref, and so too will Ve1 and Ve2,until Ve1 just barely (part 98) exceeds VH-Vp(min), as shown in waveform166 a. At this point, the voltage drop Vp across the PDACs 40 ₁ and 40 ₂becomes too small to support production of the slightly larger currentIp during the first phase pulses 30 a. Ip will thus drop slightly tomatch the value of |In|, with both becoming slightly loaded 99 (FIG.10A), and thus Icm will equal 0. This prevents capacitor Ccm fromcharging further, establishing Vcm at a level higher than Vref. Ineffect, the example 158 of FIG. 10A and example 162 a of FIG. 10B aresimilar, and would establish Vcm at the same value. It would simply takethe example 158 longer to do so because it will take longer for Vcm tobe established when Vref equals zero than when Vref is higher than zero.

If |In|>Ip as in example 162 b, a negative current Icm will initiallyflow through the capacitor Ccm 152 from ground to the case electrode Ec12. This charges the capacitor Ccm 152 with a negative voltage, whichdecreases Vcm from Vref during each pulse phase 30 a or 30 b. Thiscauses Ve1 and Ve2 referenced to Vcm to also fall. Eventually, Ve2 willjust barely (part 98) fall below Vn(min), as shown in waveform 166 b ofFIG. 10B. At this point, the voltage drop Vn across the NDACs 42 ₁ and42 ₂ becomes too small to support production of the slightly largercurrent |In|. |In| will thus drop slightly to match the value of Ip, andthus Icm will equal 0. (Again, In being loaded 99 also causes Ip tobecome loaded, since they are equal at this point, as shown in FIG.10A). Icm=0 prevents capacitor Ccm from charging further, establishingVcm at a level lower than Vref, as shown in FIG. 10B. In short, in thisexample 162 b, the fact that Icm is negative is not problematic from acircuitry standpoint because Vref is higher than zero, which allows Vcmto fall below Vref while still remaining positive.

Referring again to FIG. 9A, an optional bleed resistor Rbleed 155 isincluded in parallel with the capacitor Ccm 152. The bleed resistorRbleed 155 is preferably of a high resistance (e.g., 1 MegaOhm orhigher). Rbleed allows charge to bleed slowly off the capacitor Ccm, forexample, during periods when the passive tissue biasing circuitry is notbeing used. Furthermore, Rbleed can assist with charge balancing, whichcan be helpful in preventing loading 99 of the current pulses. Rbleedpermits a low current to flow, which current is proportional to thevoltage across the capacitor Ccm. Assume for example that the PDAC(s)are slightly stronger than the NDAC(s), i.e., that Ip>|In|initially,causing Vcm to rise. As explained earlier, Vcm will continue to increaseuntil the voltage across the stronger PDAC(s) starts to drop belowVp(min), causing Ip to drop to match |In|, thus achieving currentbalancing (and causing Icm to eventually equal 0). Beneficially,resistor Rbleed will start adding some current to the weaker NDAC(s),which may allow current balancing to happen before the PDAC(s) becomeloaded. Should this occur, there would be no loading (99) of theelectrode current, and Vcm can reach equilibrium at a lower voltage.Essentially then, Rbleed acts as a current path to boost the weaker DAC.Note that Rbleed is not shown in subsequent examples of the tissuebiasing circuitry for convenience, but could be used with any of theseexamples.

FIGS. 11A-11C further describe operation of the passive tissue biasingcircuitry 150 under different circumstances. Further described is therelevance of the modelling the tissue R with resistances Rc, R1, and R2.Such modelling is useful to consider, because the resistance betweeneach selected electrode E1 and E2 and the case electrode Ec may not bethe same, which is not surprising given the complex tissue environmentand distance between electrodes E1 and E2 and the case electrode Ec. Inparticular, R1 and R2 may vary. FIGS. 11A-11C further describe operationof the passive tissue biasing circuitry 150 if the magnitudes of Ip andIn vary, and describe how compliance voltage measurement and generationcircuitry 51 may operate to accommodate operation of the passive tissuebiasing circuitry 150. In FIGS. 11A-11C, it is assumed that Vref hasbeen set to VH/2.

In FIG. 11A, it is assumed that R1 equals R2 in the tissue model.Waveform 170 a shows the electrode node voltages Ve1 and Ve2 whenpassive tissue biasing circuitry 150 is not used (e.g., switch 154 isopened, and Vcm at the case electrodes floats). Voltage Vt within theresistance model-indicative of the tissue voltage-floats to whateverlevel would otherwise be indicated by the stimulation. In this case, itis seen that Vt is the same during each of the pulse phases 30 a and 30b. Assuming Vp(min) and Vn(min) are equal, Vt would be approximatelyVH/2. Further, assuming that compliance voltage measurement andgeneration circuitry 51 (FIG. 8B) is operating to adjust the compliancevoltage to an optimal level, Ve1 and Ve2 would be generally be tightlypinned within region 111 between Vn(min) and VH-Vp(min).

For waveforms 170 b-170 d, passive tissue biasing circuitry 150 is used(e.g., switch 154 is closed), and thus a common mode voltage Vcm ispassively established in the tissue as Ccm 152 is (possibly) charged.Ve1 and Ve2 become referenced to Vcm during each of pulse phases 30 aand 30 b.

In waveform 170 b, Ip=|In|. Icm would equal zero, and Vcm is thusestablished at approximately VH/2 (Vref), just as occurred in waveform170 a.

In waveform 170 c, it is assumed initially that Ip>|In|, as occurred inexample 162 a of FIG. 10B. Icm would initially be positive, whicheventually drives Vcm, Ve1 and Ve2 higher for the reasons alreadyexplained. This would cause Ve1 to eventually surpass VH-Vp(min).Therefore, in this example, compliance voltage measurement andgeneration circuitry 51 (FIG. 8B) operates to raise VH to alleviate thisproblem. VH would gradually be raised until Ve1 just barely passesVH-Vp(min) as shown in waveform 170 c, at which point compliance voltagemeasurement and generation circuitry 51 would stop increasing VH asshown in waveform 170 c. Ip would equal |In| at this point, Icm would bezero, and Vcm would be established at a value higher than Vref. Notethat increasing the compliance voltage VH also (further) increases Vcmin this example, because Vref (=VH/2) will also increase.

In waveform 170 d, it is assumed initially that |In|>Ip, as occurred inexample 162 b of FIG. 10B. Icm would initially be negative, eventuallydriving Vcm, Ve1, and Ve2 lower. Note that this may eventually cause Ve2to become lower than Vn(min). Again, measurement and generationcircuitry 51 can operate to raise VH and alleviate this problem. RaisingVH increases Vref (=VH/2), and hence Vcm, Ve1 and Ve2, until Ve2 is justbarely below Vn(min) as shown in waveform 170 d. |In| would equal Ip atthis point and Icm would be zero. Even though the tendency would be forVcm to decrease (Icm<0), raising VH also raises Vref, which counteractsto raise Vcm.

A comparison of waveforms 170 c and 170 d to waveform 170 b in FIG. 11Ashows that use of the passive tissue biasing circuitry 150 may warrantincreasing the value of the compliance voltage VH if the currents Ip andIn provided by the PDAC(s) and NDAC(s) are not balanced. Increasing thecompliance voltage is generally not preferred as this draws extra powerin the IPG 100, and will more quickly drain the IPG's battery 14 (FIG.1). In particular, extra headroom 101 is provided within region 111,during which the voltage drops Vn across the NDACs (waveform 170 c) andthe voltage drops Vp across the PDACs (waveform 170 d) are larger thanthose DAC require to produce the pulses with the prescribed amplitudes.However, this downside is offset by the benefit that a controlled commonmode Vcm provides when sensing neural responses in the tissue.

In FIG. 11B, it is assumed that R1 is greater than R2 in the tissuemodel. Waveform 172 a assumes that passive tissue biasing circuitry 150is not used, and thus tissue voltage Vt floats to whatever level wouldotherwise be indicated by the stimulation. In this case, it is seen thatVt is different during pulse phases 30 a and 30 b: Vt is lower duringpulse phase 30 a because more voltage is dropped across R1 than R2; andVt is higher during pulse phase 30 b when the polarity of the current isreversed.

For waveforms 172 b-172 d, passive tissue biasing circuitry 150 is used(e.g., switch 154 is closed), and thus Vcm is passively established inthe tissue as Ccm 152 is (possibly) charged. Ve1 and Ve2 are referencedto Vcm during each of pulse phases 30 a and 30 b, which in this examplecauses the waveforms to shift 171 during each of the pulse phases. Suchshifting 171 tends to draw Ve1 and Ve2 upwards during the first pulsephase 30 a, and downwards during the second pulse phase 30 b as shown inwaveform 172 b.

In waveform 172 b, it is assumed that Ip=|In|, which doesn't chargecapacitor Ccm 152. Nonetheless, referencing Ve1 and Ve2 to Vcm may causethe compliance voltage to be too low given the shifting 171, and so inwaveform 172 b it is seen that the compliance voltage has been raised(51) so that Ve1 and Ve2 are still bounded by region 111 (FIG. 8A) toprevent the resulting pulses from becoming loaded (99).

A comparison of waveforms 172 a and 172 b shows that use of the passivetissue biasing circuitry 150 may warrant increasing the value of thecompliance voltage, VH if the resistance between the active electrodesand the case electrode are not balanced. Again, while increasing VH isgenerally not desired for power consumption reasons, this downside isoffset by the benefit that a common mode voltage Vcm provides whensensing neural responses in the tissue.

In waveform 172 c, it is assumed initially that Ip>|In|, whicheventually drives Vcm, Ve1, and Ve2 higher. This may cause Ve1 tosurpass VH-Vp(min). The compliance voltage VH can therefore be raisedeven higher (51) to prevent pulse loading as shown. Again, increasingcompliance voltage VH also increases Vref, which increases Vcm evenfurther in this example.

In waveform 172 d, it is assumed |In|>Ip, which drives Vcm, and Ve1 andVe2, lower. This may cause Ve1 to become lower than Vn(min) during thesecond pulse phase 30 b. The compliance voltage VH can therefore beraised even higher (51) to prevent pulse loading, as occurred withwaveform 170 d (FIG. 11A).

Notice again by comparing waveforms 172 c and 172 d to waveform 172 bthat use of the passive tissue biasing circuitry 150 may warrant evenfurther increasing the value of the compliance voltage VH if thecurrents Ip and In provided by the PDAC(s) and NDAC(s) are not balanced,as described previously with respect to waveforms 170 b-170 d (FIG.11A). Again, this downside is acceptable given the benefit that a commonmode Vcm provides in the tissue

In FIG. 11C, it is assumed that R1 is less than R2 in the tissue model.Waveforms 174 a-174 d show conditions analogous to waveforms 172 a-172 dof FIG. 10B, which again shows how operation of the passive tissuebiasing circuitry 150 causes Ve1 and Ve2 to be referenced to Vcm asbeneficial to neural sensing, but which may also warrant increasingcompliance voltage VH (51) to prevent pulse loading.

Passive tissue biasing circuitry 150 is thus useful in passively settingVcm in the tissue to an appropriate value despite any imbalance betweenIp and In provided by the PDAC and NDAC circuitry and despite anyimbalance in resistance R1 and R2 between the active electrodes and thecase electrode Ec. As has been shown, the common mode voltage Vcmestablished at the case electrode Ec by passive tissue biasing circuitry150 will passively change from Vref provided by voltage source 153 whenthere is an imbalance, thus eventually causing the current to the case(Icm) to equal zero. This is beneficial when compared to activelydriving the case electrode to a set voltage. Actively driving aparticular voltage at the case electrode cannot guarantee that currentwill not flow through the tissue to the case electrode. Such caseelectrode currents can lead to unwanted “pocket stimulation,” meaningthat current flows from the selected electrodes to the tissue pocketwhere the case 12 is implanted. Pocket stimulation may be felt by thepatient, or may otherwise negatively affect therapy provided by theselected lead electrodes.

FIG. 12A shows another example of passive tissue biasing circuitry 200that can be used to hold tissue at a common mode voltage Vcm. Passivetissue biasing circuitry 200 essentially works similarly to passivetissue biasing circuitry 150, but includes an amplifier 180, preferablyan operational transconductance amplifier (OTA), which establishes avirtual reference voltage, Vvref, at the bottom plate of capacitor Ccm152. Note that passive tissue biasing circuitry 200 may as beforeinclude switches 154 and 156 to selectively isolate the stimulationcircuitry 28 and the passive tissue biasing circuitry 200, as explainedearlier with reference to FIG. 9A. As also explained with reference toFIG. 9B, the capacitor used in passive tissue biasing circuitry 200 cancomprise the case electrode's DC-blocking capacitor Cc 38, although thisvariation is not shown in FIG. 12A.

The OTA 180 establishes an output current, Iout that scales with adifference in the voltages at its inputs: i.e., (Vref−Vvref)*G, where Gcomprises the transconductance of the OTA 180. The OTA 180's has apositive and negative maximum output current +Iout(max) and −Iout(max).The absolute value of these maximum output currents, |Iout(max)|, is afunction of a bias current, Ibias, provided to the OTA 180:|Iout(max)|=Ibias*A, where A comprises the current gain of theamplifier. In one example, current gain A=1000 and Ibias=100 nanoAmps,which allows Iout to range from −Iout(max)=−100 microAmps to+Iout(max)=100 microAmps. Either through design of the OTA 180 oradjustment of Ibias, −Iout(max) and +Iout(max) can be adjusted todifferent values.

OTA 180 is preferably configured as a follower, in which the virtualreference voltage Vvref is fed back to the negative input of the OTA.The positive input of the OTA 180 is provided with reference voltageVref. Vref as before may be provided by a voltage source 153, and asbefore may comprise a constant or adjustable voltage preferably betweenor equal to ground (0V) and the compliance voltage (VH), such as VH/2.When connected as a follower, the OTA 180's output Vvref will equal Vrefso long as Icm is between −Iout(max) and +Iout(max), as explainedfurther below.

Operation of passive tissue biasing circuitry 200 can be understood withthe assistance of the graphs in FIG. 12A. Given the polarity with whichIout is defined in FIG. 12A, Iout=Icm when Icm is between −Iout(max) and+Iout(max). When in this range, Icm simply passes as Iout through theOTA 180. Because the output current of the OTA 180 is not exceeded inthis range, virtual reference voltage Vvref remains constant and equalto Vref.

Examples 190 a and 190 b show operation when Icm is positive and below+Iout(max). Example 190 a shows a small mismatch between Ip and |In|,and thus a relatively small current Icm. At this current level, Vcminitially increases as capacitor Ccm is charged, while Vvref stays equalto Vref. Eventually (as the pulses repeat), Vcm stabilizes at a constantlevel, as explained earlier (FIGS. 10A-10B). Example 190 b shows ahigher mismatch between Ip and |In|, and thus a higher current Icm. Thiswill charge the capacitor Ccm faster, and Vcm will rise faster and willeventually be established at a higher value. Although not shown, itshould be understood that negative values for Icm would establish Vcm atlevel below Vref.

If the mismatch between Ip and |In| is large, such that Icm would exceed+Iout(max) as in example 190 c, the OTA 180 will only be able to draw+Iout(max), thus capping Icm to this value. Having the OTA 180 limit Icmprovides a benefit to passive tissue biasing circuitry 200 of FIG. 12A,because limiting Icm limits “pocket stimulation,” which as explainedearlier can be caused when unwanted current flows to the tissue pocketwhere the case 12 is implanted. In this regard, the OTA 180 can bedesigned to set +Iout(max) and −Iout(max) to appropriate values to limitthe potential magnitude of pocket stimulation.

Returning to example 190 c, because the OTA 180 cannot accommodate allof the excess current, Vcm and Vvref will initially be pulled above Vrefto a value Vvref(max), which will vary in magnitude as further pulsesare issued. (Again, Vref can be set to VH/2 to allow for pulling Vvrefdownward if Icm is negative, with the OTA 180 limiting Icm to−Iout(max)). Capacitor Ccm will then start to charge in acurrent-limited fashion (with Icm=+Iout(max)), causing Vcm to increaseand Vvref to decrease. As the capacitor Ccm continues to charge upon theissuance of subsequent pulses, and as shown further in FIG. 12B, Vcmwill continue to rise, and Vvref will continue to fall. As notedearlier, Vcm rising will cause the electrode node voltages (e.g., Ve1and Ve2 to rise), eventually to a point at which one of the waveformswill start to breach VH-Vp(min), which causes dominant current Ip tofall to match |In|, as explained earlier (FIGS. 10A-10B). At this pointIcm will equal zero, halting further charging of the capacitor, Ccm, andestablishing Vcm at a value below VH-Vp(min). Note also that Vvref willreturn to Vref when Icm equals zero. Again, negative values for Icmwould establish Vcm at level below Vref, but above Vn(min).

FIG. 13A shows another example of passive tissue biasing circuitry 250(switches 154 and 156 not shown) which adds optional additionalcircuitry for monitoring the virtual reference voltage, Vvref. Switches154 and 156 are not shown for simplicity.

A window comparator as logic circuitry is provided comprising twocomparators 182 a and 182 b. Each comparator 182 a and 182 b receivesVvref and a reference voltage that sets a window 173 around Vref. In theexample shown, window 173 is 200 mV wide, and is set from Vref−100 mV toVref+100 mV. Vref+100 mV is provided to comparator 182 a, while Vref−100 mV is provided to comparator 182 b. Voltages Vref−100 mV andVref+100 mV may be provided by voltage sources similar to source 153that produces Vref, although such additional sources are not shown. Byconnecting Vvref, Vref+100 mV, and Vref−100 mV to the appropriatepositive and negative inputs of the comparators, comparator 182 a'soutput X will equal a ‘1’ if Vvref>Vref+100 mV, and comparator 182 b'soutput Y will equal a ‘1’ if Vvref<Vref−100 mV. Outputs X and Y willequal ‘0’ if Vvref is between Vref+100 mV and Vref −100 mV. A plus-minusvalue of 100 mV for window 173 is just one example, and a differentvalue could be used. An output providing at least one indication thatVvref has exceeded the Vref+100 mV or has fallen below the Vref−100 mVcould also be used.

Outputs X and Y are provided to control circuitry 102, allowing virtualreference voltage Vvref to be monitored at appropriate times asdiscussed further below. Such monitoring is useful in a couple ofdifferent respects. First, it allows the control circuitry 102 to decidewhen neural response sensing is best performed in the IPG 100, which canbe effectuated by having control circuitry issue sensing enable signalS(en), as explained further with reference to FIGS. 14A and 14B.

Second, monitoring Vvref is also useful to allow the control circuitry102 to decide whether the compliance voltage VH should be raised.Raising the compliance voltage VH can be effected by asserting enablesignal VH(en2), which can be sent to the input VH(en) of the PWM 53 ofthe compliance voltage measurement and generation circuitry 51 (FIG. 8B)which as explained earlier will activate VH regulator 49 to raise thecompliance voltage. In this regard, the VH regulator 49 may be activatedat its input either by enable signal VH(en1) provided by the measurementcircuitry in the compliance voltage measurement and generation circuitry51 as already explained, or by the assertion of VH(en2). Thisalternative is particularly useful because VH(en1) can operate when thepassive tissue biasing circuitry 250 is not operating (switch 154 isopen), while VH(en2) can operate when the passive tissue biasingcircuitry 250 is operating (switch 154 is closed). OR gate 184 in FIG.13A can be used to process the two enable signals VH(en1) and VH(en2)and assert input VH(en) when either is active. In another example, theVH regulator 49 may be activated exclusively by enable signal VH(en2),mooting the need for measurement circuitry in the compliance voltagemeasurement and generation circuitry 51.

FIG. 13B explains the operation of passive tissue biasing circuitry 250and how control circuitry 102 can be used to issue control signals S(en)to enable neural sensing and VH(en2) to increase the compliance voltage.It is useful that the control circuitry 102 review the status of outputsX and Y from the window comparator during both first 30 a and second 30b phases of the biphasic pulses, as either pulse phase may provideinformation relevant to neural sensing or compliance voltage adjustment.Note that control circuitry 102 may know when the first and secondpulses phases 30 a and 30 b are occurring, and thus when outputs X and Yshould be sampled, because it may program the stimulation circuitry 28with this timing information. Otherwise, the control circuitry 102 canreceive one or more control signals 186 (tp1, tp2) from the stimulationcircuitry 28 indicative of when stimulation is occurring during thefirst and second pulse phases 30 a and 30 b. Control signals tp1 and tp2may be asserted to inform the control circuitry 102 when it is to sampleoutputs X and Y, which may be programmed to occur nearer to the ends ofthe pulse phases 30 a and 30 b when charging of the DC-blockingcapacitors 38 is most severe, and hence when the electrode node voltages(e.g., Ve1 and Ve2) are most likely to breach region 111 (see, e.g.,FIG. 7B).

Example 202 a in FIG. 13B occurs when Icm passing through the capacitorCcm is within the OTA 180's output current limits during both pulsephases, i.e., when −Iout(max)<Icm<+Iout(max). During this example 202 a,Vvref would be within window 173, and generally equal to Vref, andoutputs X and Y would equal ‘0’ during both pulse phases. Vcm would besteady, and hence control circuitry 102 can enable sensing at this timeby asserting S(en). Moreover, there is no reason to believe thatcompliance voltage VH is insufficient at this point so as to warrantenabling the VH regulator 49 per VH(en2).

During example 202 b, a significant positive current Icm>+Iout(max)occurs during both pulse phases 30 a and 30 b. During this example 202b, Vvref would be outside of window 173, i.e., Vvref>Vref+100 mV. OutputX would therefore equal ‘1’ during both pulse phases, while output Ywould equal ‘0.’ Vcm would not be steady, as shown in FIG. 12B. Hence,control circuitry 102 would disable sensing at this time by deassertingS(en). There is no still reason to believe that compliance voltage VH isinsufficient at this point. Instead, the capacitor Ccm may merely becharging to a steady state, as occurred in FIG. 12B. Therefore, thecontrol circuitry 102 would thus deassert VH(en2).

Example 202 c is essentially the opposite of example 202 b, having asignificant negative current Icm<−Iout(max) during both pulse phases 30a and 30 b. During this example 202 c, Vvref would be outside of window173, i.e., Vvref<Vref+100 mV. Output X would therefore equal ‘0’ duringboth pulse phases, while output Y would equal ‘1.’ Vcm would not besteady, because it would be in the process of decreasing below VrefHence, control circuitry 102 would disable sensing at this time bydeasserting S(en). There is again no reason to believe that compliancevoltage VH is insufficient at this point, because the capacitor Ccm maystill be charging to a steady state. Therefore, the control circuitry102 would thus deassert VH(en2).

During example 202 d, it is seen that Icm is significantly positive(>+Iout(max)) during the first pulse phase 30 a and significantlynegative (<−Iout(max)) during the second pulse phase. During the firstpulse phase 30 a, Vvref would be higher than Vref+100 mV, and output Xwould equal ‘1’, while output Y would equal ‘O’. During the second pulsephase 30 b, Vvref would be lower than Vref−100 mV, and these logicstates are flipped, with output X equaling ‘0’ and output Y equaling‘1.’ Vcm would not be steady, and thus control circuitry 102 woulddisable sensing at this time by deasserting S(en). Moreover, thisexample 202 d would not suggest that capacitor Ccm is merely on its wayto being charged to a steady state, as the current Icm flowing throughthe capacitor is reversed during the two pulse phases. Instead, thisexample would suggest that the compliance voltage is insufficient: theNDACs are apparently loaded (Vn<Vn(min) during the first pulse phase 30a (when Ip predominates), and the PDACs are apparently loaded(Vp<Vp(min)) during the second pulse phase 30 a (when In predominates).This suggests that the electrode node voltages (e.g., Ve1 and Ve2)cannot stay within region 111 (FIG. 8A). Therefore, the controlcircuitry would assert VH(en2) during this example 202 d.

Example 202 e is essentially the opposite of example 202 d, with thepredominance in Icm flipped during the two pulse phases. Again, thecontrol circuitry 102 would deassert S(en) and assert VH(en2).

FIGS. 14A and 14B show how the generation of the common mode voltage Vcmcan be used to assist in sensing neural responses in the tissue. In bothof these figures, the sense amp 110 used to sense the neural responsecan be enabled to sense only when an enable signal, S(en), is asserted.This enable signal can be generated by the control circuitry 102 asexplained with reference to FIGS. 13A and 13B, or could be generated inother manners and at other times.

FIG. 14A shows single ended sensing (S) of a neural response at aselected electrode E6 as explained earlier. Electrode node voltage Ve6is provided to one input of the sense amp 110, while the other inputreceives Vcm as generated at the case electrode. Ve6 would also bereferenced to Vcm present in the tissue. Because Vcm is stable in thetissue, the sense amp 110 is better able to reject this voltage, andsense the small signal neural response.

FIG. 14B shows differential sensing (S1 and S2) at different electrodesE5 and E6. Electrode node voltages Ve5 and Ve6 are provided to the inputof the sense amp 110, both of which are referenced to Vcm. Again, thisassists in sensing the small signal neural response.

The disclosed examples of passive tissue biasing circuitry areparticularly useful in sensing neural responses, but could be useful inother context as well where it is beneficial that the common modevoltage in the tissue be set or well controlled. Further, while thepassive tissue biasing circuitry has been shown as operating while anytwo electrodes are selected (e.g., E1 and E2), the circuitry can alsooperate if any two or more electrodes are selected for stimulation(e.g., electrodes E1 and E2 as anodes outputting a summed anodic current+I, and electrode E3 as a cathode outputting cathodic current −I).

To this point in the disclosure it has been assumed that the caseelectrode Ec 12 comprises the electrode that is used by the passivetissue biasing circuitry to set the common mode voltage Vcm in thetissue. However, any electrode, including the lead-based electrodes 16(FIG. 1), could also be used for this purpose. FIG. 15 shows thisalternative to passive tissue biasing circuitry 300, and comprises anexample in which any electrode, such as any lead-based electrode 16 orthe case electrode Ec 12, can be chosen to set the common mode voltage,Vcm. The example shown in FIG. 15 corresponds generally to circuitry 200(FIG. 12A), although any of 150 (FIG. 9A), 150′ (FIG. 9B), or 250 (FIG.13A) could employ the alternative circuitry of FIG. 15.

In FIG. 15, switches 154 and 156 have each been expanded to comprise amatrix of switches, with one switch 154 and one switch 156 associatedwith each of the lead-based electrodes (E1, E2, etc.) and the caseelectrode Ec. Switches 154 and switches 156 are similar in functionalityto the individual switches 154 and 156 described earlier. Switches 156are used to couple each electrode Ei to the stimulation circuitry 28(not shown) via electrode nodes ei, while switches 154 are used tocouple each electrode Ei to the common mode capacitor Ccm. Thus, in thisexample, the common mode capacitor Ccm is shared by the electrodes; inanother example, each electrode could include its own dedicatedcapacitor for setting Vcm.

In the example shown at the bottom of FIG. 15, it is assumed thatelectrodes E1 and E2 have been selected as active to provide biphasicstimulation (I) to the tissue, while electrode E3 will provide thecommon mode voltage, Vcm. Switches 156 coupled to active electrodes E1and E2 are thus closed (control signals A1 and A2 are asserted) toconnect these electrodes to the stimulation circuitry 28. Because it isinconsistent to also provide Vcm at these active electrode nodes, theirswitches 154 are opened (control signals B1 and B2 are deasserted) todisconnect these electrodes from the capacitor Ccm. By contrast,electrode E3 which will establish the common mode voltage Vcm for thetissue will have its switch 154 closed (control signal B3 is asserted)to connect E3 to the capacitor Ccm. Because it is inconsistent to alsodrive electrode E3 with the stimulation circuitry 28, its switch 156 isopened (control signals A3 is deasserted). All other switches notassociated with electrodes E1, E2, or E3 can be opened, as they are notin this example involved in either driving a tissue current or providinga common mode voltage Vcm.

Note that more than one electrode can be selected to provide the commonmode voltage. For example, electrodes E3 and E4 can be selected to bothprovide Vcm (asserting B3 and B4), or electrodes E3, E4, and the caseelectrode Ec can all be selected to provide Vcm (asserting B3, B4, andBc). Electrode(s) selected to sense the neural response-such aselectrode E6 in the example of FIG. 15—would not be selected toparticipate in providing Vcm to the tissue. That is, E6's switch 154would be open (B6 deasserted) as would its switch 156 (A6 deasserted)because E6 would not be driven by the stimulation circuitry 28 whilesensing.

Providing Vcm to an electrode closer to those being used for stimulationmay assist in referencing the electrode node voltages to Vcm.Furthermore, allowing a non-case electrode 16 to provide Vcm allows thecase electrode Ec 12 to be actively driven (Ac asserted; Bc deasserted),such as during monopolar stimulation, while still providing the benefitsthat Vcm generation provides.

Although not illustrated, the IPG 100 could include one or more specialelectrodes anywhere on the device for setting Vcm, which electrode(s)may be dedicated to Vcm generation and not useable to providestimulation to the tissue, R.

Although particular embodiments of the present invention have been shownand described, the above discussion is not intended to limit the presentinvention to these embodiments. It will be obvious to those skilled inthe art that various changes and modifications may be made withoutdeparting from the spirit and scope of the present invention. Thus, thepresent invention is intended to cover alternatives, modifications, andequivalents that may fall within the spirit and scope of the presentinvention as defined by the claims.

What is claimed is:
 1. An implantable stimulator device, comprising: aplurality of electrode nodes, each electrode node configured to becoupled to one of a plurality of electrodes configured to contact apatient's tissue; a case configured for implantation in the patient'stissue, wherein the case contains stimulation circuitry configured toprovide pulses at at least two of the electrode nodes to create astimulation current through the patient's tissue; and a capacitanceconfigured to be coupled between at least one of the plurality ofelectrodes and a first reference voltage produced inside the case whenthe stimulation circuitry is providing the pulses to the at least twoelectrode nodes, wherein the capacitance is configured to provide acommon mode voltage to the tissue at the at least one electrode.
 2. Theimplantable stimulator device of claim 1, wherein the case isconductive, wherein the conductive case comprises the at least oneelectrode.
 3. The implantable stimulator device of claim 1, wherein theat least one electrode is configured to be selectable from the pluralityof electrodes.
 4. The implantable stimulator device of claim 1, whereinthe capacitance comprises one or more capacitors.
 5. The implantablestimulator device of claim 1, wherein the stimulation circuitry isfurther configured to provide pulses to the at least one electrode,wherein the capacitance is configured to be uncoupled between the atleast one electrode and the first reference voltage when the stimulationcircuitry is providing the pulses to the at least one electrode.
 6. Theimplantable stimulator device of claim 1, further comprising a voltagesource configured to produce the first reference voltage.
 7. Theimplantable stimulator device of claim 1, wherein the stimulationcircuitry is configured to be powered by a compliance voltage, andwherein the first reference voltage is between the compliance voltageand a ground.
 8. The implantable stimulator device of claim 7, whereinthe first reference voltage is configured to scale with the compliancevoltage.
 9. The implantable stimulator device of claim 1, furthercomprising an amplifier configured to produce the first referencevoltage.
 10. The implantable stimulator device of claim 9, wherein theamplifier comprises a first input and a second input, wherein theamplifier is configured as a follower in which the first referencevoltage is provided to the first input, and wherein a second referencevoltage is provided to the second input.
 11. The implantable stimulatordevice of claim 10, further comprising a voltage source configured toproduce the second reference voltage.
 12. The implantable stimulatordevice of claim 11, wherein the stimulation circuitry is configured tobe powered by a compliance voltage, wherein the second reference voltageis between the compliance voltage and a ground.
 13. The implantablestimulator device of claim 12, wherein the second reference voltage isconfigured to scale with the compliance voltage.
 14. The implantablestimulator device of claim 10, wherein the amplifier is configured tomaintain the first reference voltage equal to the second referencevoltage if a current through the capacitance is between a minimum andmaximum output current of the amplifier.
 15. The implantable stimulatordevice of claim 10, further comprising logic circuitry configured toissue at least one indication that the first reference voltage exceeds afirst threshold or falls below a second threshold.
 16. The implantablestimulator device of claim 15, further comprising control circuitryconfigured in response to the at least one indication to issue an enablesignal indicating when a neural response in the tissue in response tothe stimulation current can be sensed at at least one of the pluralityof electrode nodes.
 17. The implantable stimulator device of claim 16,wherein the stimulation circuitry is powered by a compliance voltage,wherein the control circuitry is configured in response to the at leastone indication to issue an enable signal indicating when the compliancevoltage should be increased.
 18. The implantable stimulator device ofclaim 1, further comprising at least one sense amplifier configured tosense a neural response in the tissue in response to the stimulationcurrent when the capacitance is configured to provide the common modevoltage to the tissue at the at least one electrode.
 19. The implantablestimulator device of claim 18, wherein the at least one sense amplifiercomprises a first input and a second input, wherein the at least onesense amplifier is configured to receive one of the electrode nodes atits first input.
 20. The implantable stimulator device of claim 19,wherein the at least one sense amplifier is configured to receive thecommon mode voltage at its second input, or is configured to receiveanother one of the electrode nodes at its second input to differentiallysense the neural response between the one electrode node and the anotherelectrode node.